Angiotensin retains sodium by dephosphorylating mineralocorticoid receptors in renal intercalated cells.

@article{Funder2013AngiotensinRS,
  title={Angiotensin retains sodium by dephosphorylating mineralocorticoid receptors in renal intercalated cells.},
  author={John W. Funder},
  journal={Cell metabolism},
  year={2013},
  volume={18 5},
  pages={
          609-10
        }
}
In this issue of Cell Metabolism, Shibata et al. (2013) show that in renal intercalated cells mineralocorticoid receptors phosphorylated on serine 843 are rendered active by angiotensin-induced dephosphorylation. This finding represents a novel mechanism for regulating nuclear receptor activity, and explains the balance between Na-Cl reabsorption in response to volume depletion and K(+) excretion in response to potassium loading. 
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Cell Metab

  • S. Shibata, J. Rinehart, +6 authors R. P. Lifton
  • 18, this issue, 660–671.
  • 2013
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